Abstract
Utilizing a murine model of S. pneumoniae infection and restraint stress, we determined how corticotropin releasing hormone (CRH-R) receptors impacts disease. CRH-R1 (antalarmin) and CRH-R2 (astressin2B) antagonists were administered intraperitoneally prior to restraint stress followed by pulmonary S. pneumoniae infection. CRH-R1 inhibition is not protective against pneumococcal disease induced by stress. Conversely, CRH-R2 inhibition attenuates stress-induced bacterial growth and significantly prevented severe sepsis. Neutrophillic responses were associated with CRH receptor-specific disease outcome providing a potential cellular target for stress-induced susceptibility to the development of severe pneumococcal disease. CRH receptor-mediated effects on immune responses could prove valuable for novel therapeutics.
Original language | English |
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Pages (from-to) | 57-65 |
Number of pages | 9 |
Journal | Journal of Neuroimmunology |
Volume | 237 |
Issue number | 1-2 |
DOIs | |
State | Published - 15 Aug 2011 |
Keywords
- Corticotropin releasing hormone
- Lung
- Neuroimmune
- Neutrophils
- Restraint stress
- S. pneumoniae
- Sepsis